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Crohn's disease: gross appearance and histology

Linear ulcers and normal mucosa interspersed --> cobblestone appearance. Creeping fat.Histo: non-caseating granulomas, lymphoid inflammatory infiltrate (Th1 mediated)


What cell type mediates Crohn's disease?



Describe squamous cell carcinoma histology. What is the importance of keratin?

Nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct bordersKeratinization means that the tumor is poorly differentiated --> poor prognosis.


What 3 organisms are most common causes of esophagitis? What patients is this found in?

Found in immunocompromised. Candida albicans, HSV-1, and CMV.


Gross and histologic features: Candida esophagitis

Gross: white pseudomembranesHisto: yeast cells and pseudohyphae that invade mucosal cells


Gross and histologic features: HSV esophagitis

Gross: "punched out" ulcersHisto: eosinophilic intranuclear inclusions in multinuclear squamous cells at margins of ulcers.


Gross and histologic features: CMV esophagitis

Gross: linear ulcerations

Histo: intranuclear and cytoplasmic inclusions


Where is H. pylori found in greatest concentration in the GI tract?

Prepyloric area of the gastric antrum (even if it is a duodenal ulcer)


Presentation of carcinoid syndrome

Dyspnea, wheezing, cutaneous flushing, diarrhea. Maybe right sided valvular disease


Tx of carcinoid syndrome

Resection and somatostatin analogue, aka octreotide (inhibits secretion of many hormones)


Where should you biopsy for Hirshprung's?

Must go down to the submucosa to see the lack of ganglion cells - mucosa alone is not enough.

Also this is for the constricted portion, not dilated.


Abetalipoproteinemia presentation

Presents in early childhood. Failure to thrive, steatorrhea, malabsorption, acanthocytosis, ataxia, night blindness.


Abetalipoproteinemia: labs and biopsy

Low plasma triglycerides, low cholesterol, no chylomicrons, VLDLs, apoBs. Poor absorption of ADEK.


Classification of adenomatous polyps

Tubular: smaller, pedunculated, dysplastic mucosal cells form tubular-shaped glands.

Villous: larger, sessile, dysplastic epithelial cells form villi-like projections. Velvety or cauliflower like masses. Increased risk of adenocarcinoma.


Difference between erosions and ulcers

Erosions do not fully extend through the muscularis mucosa (but they can reach it)

Ulcers penetrate through the mucosa into submucosa.


What is the first event in the pathogenesis of acute appendicitis?

lumen obstruction


Histology of Crohn's disease

Non-caseating granulomas, lymphoid aggregates


Multiple hemorrhagic polypoidal lesions, spindle cells with surrounding blood vessel proliferation in the setting of untreated HIV. Dx?

Kaposi's sarcoma


Kaposi's sarcoma: colonoscopy findings, biopsy findings, other organ system involvement

Colonoscopy: red/violet, flat maculopapular lesions or hemorrhagic nodules
Biopsy: spindle-shaped tumor cells with small vessel proliferation.

Endothelial malignancy in skin, mouth, GI tract, respiratory tract, associated with HHV-8 and HIV


CMV colonoscopy and biopsy findings

Colonoscopy: multiple ulcers, mucosal erosions
Biopsy: cytomegalic cells with inclusion bodies


Cryptosporidium colonoscopy and biopsy findings

C: nonulcerative inflammation
B: Basophilic clusters on surface of intestinal mucosal cells


Characteristics of colitis-associated colorectal carcinoma

Affects younger patients, multifocal, progresses from flat non-polypoid lesions, mucinous or signet ring histology, early p53 and late APC mutations, disease is dependent on length of colitis (>10 years)


Congenital pyloric stenosis: "olive sized" mass is from:

smooth muscle hypertrophy


Systemic mastocytosis: cause and effects

Mast cell proliferation in marrow and organs.
Syncope, flushing, hypotension, tachycardia, bronchospasm, pruritis.
GI symptoms from increased gastric acid secretion: diarrhea (inactivated pancreatic enzymes), nausea, vomiting, cramps.


Which gastritis is associated with the antrum?

Type B - H. pylori


Differentiate between acute and chronic gastritis

Acute = neutrophil dominant
Chronic = lymphocyte and plasma cell predominant


Presentation of chronic gastritis

epigastric abdominal pain, occasional nausea, not related to food intake, inflammatory infiltrate


Presentation of Crohn's

Fever, right lower quadrant pain (terminal ileitis), diarrhea, involves GI tract not stomach!


Damage seen in pernicious anemia

Immune mediated destruction of gastric mucosa --> Chronic atrophic gastritis. Loss if IF-secreting cells (B12 deficiency, megaloblastic anemia), lymphocytic and plasma cell infiltration, megaloblastic changes


What stimulus causes parietal cell proliferation?

Gastrin: facilitates HCl secretion, AND has a trophic effect causing proliferation and hyperplasia

Seen in Zollinger-Ellison syndrome